title: Endometrial signaling pathways during ovarian stimulation for assisted reproduction technology.
abstract: OBJECTIVE
  To determine the effects of different hormonal levels on endometrial biochemical development during ovulation induction for assisted reproduction technology (ART) cycles.
  
  
  METHODS
  Prospective controlled study.
  
  
  METHODS
  University center.
  
  
  METHODS
  Nine women during a natural cycle (control) and 9 oocyte donors (treated) during an ART cycle.
  
  
  METHODS
  At the time consistent with day 3 embryo transfer (LH+5 in control, hCG+5 in treated), transvaginal ultrasound, endometrial biopsy, and blood sampling were performed. Real-time reverse-transcription polymerase chain reaction was used to measure mRNA levels for insulin receptor (InsR), type I IGF receptor (IGFRI), prolactin receptor (PRL-R), androgen receptor (AR), TSH receptor (TSHR), nuclear receptors for T3 and T4 (TRα1, TRα2, and TRβ1), iodothyronine deiodinase (DIO2), and 1,25-dihydroxyvitamin D3 receptor (VDR) in the endometrial tissue.
  
  
  METHODS
  Biochemical endometrial development.
  
  
  RESULTS
  IGFRI mRNA levels were 69% lower in treated patients than in control subjects, 0.12 ± 0.005 pg/μg RNA versus 0.39 ± 0.01 pg/μg RNA. TSHR mRNA was 57% lower, 2.6 ± 0.1 fg/μg RNA versus 6.0 ± 0.2 fg/μg RNA. TRα1 and TRα2 mRNA did not change, but TRβ1 mRNA levels were 63% higher. DIO2 mRNA was 63% lower, 1.2 ± 0.07 pg/μg RNA versus 3.2 ± 0.2 pg/μg RNA. InsR mRNA levels, despite being 68% lower in treated patients, did not reach significance, and PRL-R, AR, and VDR did not significantly change.
  
  
  CONCLUSIONS
  Exposure of the endometrium to ovarian stimulation appears to influence insulin and thyroid hormone signaling pathways in the decidua at day 3 embryo transfer, whereas prolactin, androgen, and vitamin D pathways are uninfluenced. These findings echo the known delayed endometrial maturation during ovarian stimulation.
authors.affiliation: Department of Obstetrics and Gynecology, University of Tennessee Health Science Center, Memphis, Tennessee 38162, USA. ldetti@uthsc.edu
authors.forename: Laura
authors.initials: L
authors.lastname: Detti
authors.forename: Rebecca A
authors.initials: RA
authors.lastname: Uhlmann
authors.forename: Nicole M
authors.initials: NM
authors.lastname: Fletcher
authors.forename: Michael P
authors.initials: MP
authors.lastname: Diamond
authors.forename: Ghassan M
authors.initials: GM
authors.lastname: Saed
mesh_terms: D000328:Adult; D004717:Endometrium / Q000187:drug effects* / Q000378:metabolism*; D005260:Female; D005300:Fertility Agents, Female / Q000008:administration & dosage*; D015870:Gene Expression / Q000187:drug effects; D006728:Hormones / Q000097:blood; D006801:Humans; D010062:Ovulation Induction; D011388:Prolactin / Q000097:blood; D017526:Receptor, IGF Type 1 / Q000235:genetics / Q000378:metabolism; D018160:Receptors, Cytoplasmic and Nuclear / Q000235:genetics / Q000378:metabolism; D011981:Receptors, Prolactin / Q000235:genetics / Q000378:metabolism; D011989:Receptors, Thyrotropin / Q000235:genetics / Q000378:metabolism; D027724:Reproductive Techniques, Assisted; D015398:Signal Transduction / Q000187:drug effects / Q000235:genetics; D055815:Young Adult
chemical_list: D005300:Fertility Agents, Female; D006728:Hormones; D018160:Receptors, Cytoplasmic and Nuclear; D011981:Receptors, Prolactin; D011989:Receptors, Thyrotropin; D011388:Prolactin; D017526:Receptor, IGF Type 1
keywords: ART; Endometrium; GnRH-antagonist; decidua; development; hormone receptors; real time RT-PCR